Elizabeth R. Tor

Type C botulism in dairy cattle from feed contaminated with a dead cat

Four hundred twenty-seven of 441 adult Holstein dairy cattle from a 1,200-cow dairy died over a 1-week period during early spring 1998. Affected animals were from 4 late lactation pens, one of which included the bull string. Signs included weakness, recumbency, watery diarrhea, and death. Eighty animals from the 4 pens were dead approximately 8 hours after the first ill cows were noted. Affected cows would collapse on stimulation and extend all 4 limbs with moderate rigidity. Several lacked lingual tonus and had abdominal breathing patterns. The animals had been fed a load of total mixed ration that included a rotten bale of oat hay containing a dead cat. No common toxicants were identified, and pathologic examination revealed no consistent lesions. Testing of tissue from the cat carcass found in the feed sample using mouse protection bioassay identified the presence of type C botulinum toxin. Samples of feed, tissue from affected animals, cat tissue from feed, milk, and serum were also tested using an enzyme-linked immunosorbent assay (ELISA) specific for type C botulinum. Two samples of rumen contents were tested and found to be positive for botulism by ELISA, and 1 of 3 liver samples had a weak positive finding. No botulinum toxin was found in milk or sera using the ELISA.

Diagnosis of Anatoxin-a Poisoning in Dogs from North America

Anatoxin-a, a toxin produced by several genera of blue-green algae, is considered a potent neurotoxin. Ingestion of water contaminated with the toxin results in acute neurological signs and often death. This report describes fatal cases of anatoxin-a ingestion in 6 dogs, with confirmation of anatoxin-a exposure by liquid chromatography/tandem mass spectrometry (LC-MS/MS/MS). In 1 outbreak, 3 dogs developed seizures and died within an hour after swimming in a river in California, while the other outbreak involved 3 dogs that died within 1 hour after swimming in a pond in Ontario. Anatoxin-a poisoning is rarely reported in dogs as a cause of acute neurological signs and death. However, increased occurrences of blue-green algae blooms in North America make this neurotoxin an important consideration in the diagnosis of sudden death associated with environmental water exposure. This brief communication reports on the isolation and detection of anatoxin-a from environmental water sources and the stomach contents of North American dogs dying of acute neurotoxicosis. This demonstrates the first documented cases of anatoxin-a poisoning in dogs in North America and the importance of LC-MS/MS/MS in identifying neurotoxins responsible for sudden death in cases of suspected blue-green algae toxicosis; especially those cases showing no gross or histological lesions.

Diagnosis of Oleander Poisoning in Livestock

Since mid- 1989, 37 cases of oleander poisoning in livestock have been diagnosed at the California Veterinary Diagnostic Laboratory System. The most frequent source for oleander exposure was plant clippings. Sudden death was the most common presenting complaint. Other signs reported included diarrhea, pulmonary edema, tachycardia, cardiac arrhythmias, colic, and lethargy. In the past, a presumptive diagnosis of oleander poisoning could be based only on matching clinical signs with evidence of consumption of oleander. A new 2 dimensional Thin-layer chromatography analysis of ingesta for oleandrin and an awareness of lesions in heart muscle have greatly improved the ability to diagnose oleander toxicosis.

Diagnosis of Taxus (Yew) Poisoning in a Horse

A 2-year-old bay Thoroughbred colt was found dead overnight in its stall without a known history of any illness, existing disease, or toxicant exposure. No information on the clinical signs before this animals death was reported. A full necropsy was performed the next morning and revealed a mild to moderate degree of endocardial hemorrhages in both ventricles. Microscopic examination of the heart showed an acute mild mutifocal necrosis of papillary muscles and ventricles. The stomach content contained approximately 2% Taxus alkaloids as determined by gas chromatography/mass spectrometry. In the past, diagnosis of Taxus poisoning has been mainly based on history of exposure and the presence of plant parts in the gastrointestinal tract. Pathological lesions associated with Taxus poisoning have not been published for horses. Therefore, this is the first report of cardiac lesions in a horse after lethal exposure to Taxus. On the basis of these findings, it is suggested that Taxus exposure needs to be considered in the differential diagnosis of horses that die suddenly or have cardiac lesions suggestive of Taxus exposure, even if intact plant parts are not identified in the stomach by the naked eye.

Treatment and diagnosis of a dog with fulminant neurological deterioration due to anatoxin‐a intoxication

OBJECTIVE To describe the clinical features, treatment, diagnostic work-up, and outcome of a dog with acute neurologic signs subsequent to algal toxin exposure. CASE SUMMARY A Golden Retriever was presented for evaluation of acute onset of paraparesis after swimming in a man-made pond in early June and ingesting algae from a nearby bucket. The dog was anxious, had mild ptyalism, and when excited, developed generalized self-limiting tremors that progressed to generalized fasciculations and lateral recumbency. The dog was treated with activated charcoal and crystalloid fluids. Two hours after the presentation, the dog acutely decompensated and was ultimately euthanized. Gastric contents, bucket contents, pond water, bile, and urine were positive for anatoxin-a. NEW OR UNIQUE INFORMATION PROVIDED Anatoxin-a intoxication is rarely confirmed in dogs but should be considered as a differential diagnosis in any dog with acute neurologic signs. We report the first successful detection of anatoxin-a in urine and bile of a dog exposed to blue green algae. This new test provides an enhanced diagnostic tool in suspect cases and has possible therapeutic implications in dogs.Abstract Objective – To describe the clinical features, treatment, diagnostic work-up, and outcome of a dog with acute neurologic signs subsequent to algal toxin exposure. Case Summary – A Golden Retriever was presented for evaluation of acute onset of paraparesis after swimming in a man-made pond in early June and ingesting algae from a nearby bucket. The dog was anxious, had mild ptyalism, and when excited, developed generalized self-limiting tremors that progressed to generalized fasciculations and lateral recumbency. The dog was treated with activated charcoal and crystalloid fluids. Two hours after the presentation, the dog acutely decompensated and was ultimately euthanized. Gastric contents, bucket contents, pond water, bile, and urine were positive for anatoxin-a. New or Unique Information Provided – Anatoxin-a intoxication is rarely confirmed in dogs but should be considered as a differential diagnosis in any dog with acute neurologic signs. We report the first successful detection of anatoxin-a in urine and bile of a dog exposed to blue green algae. This new test provides an enhanced diagnostic tool in suspect cases and has possible therapeutic implications in dogs.

A Collaborative Study: Determination of Mycotoxins in Corn, Peanut Butter, and Wheat Flour Using Stable Isotope Dilution Assay (SIDA) and Liquid Chromatography–Tandem Mass Spectrometry (LC-MS/MS)

A collaborative study was conducted to evaluate stable isotope dilution assay (SIDA) and LC-MS/MS for the simultaneous determination of aflatoxins B1, B2, G1, and G2; deoxynivalenol; fumonisins B1, B2, and B3; ochratoxin A; HT-2 toxin; T-2 toxin; and zearalenone in foods. Samples were fortified with 12 13C uniformly labeled mycotoxins (13C-IS) corresponding to the native mycotoxins and extracted with acetonitrile/water (50:50 v/v), followed by centrifugation, filtration, and LC-MS/MS analysis. In addition to certified reference materials, the six participating laboratories analyzed corn, peanut butter, and wheat flour fortified with the 12 mycotoxins at concentrations ranging from 1.0 to 1000 ng/g. Using their available LC-MS/MS platform, each laboratory developed in-house instrumental conditions for analysis. The majority of recoveries ranged from 80 to 120% with relative standard derivations (RSDs) <20%. Greater than 90% of the average recoveries of the participating laboratories were in the range of 90-110%, with repeatability RSDr (within laboratory) < 10% and reproducibility RSDR (among laboratory) < 15%. All Z scores of the results of certified reference materials were between -2 and 2. Using 13C-IS eliminated the need for matrix-matched calibration standards for quantitation, simplified sample preparation, and achieved simultaneous identification and quantitation of multiple mycotoxins in a simple LC-MS/MS procedure.

Total Cholinesterase Activity in Discrete Brain Regions and Retina of Normal Horses

2,3,5,7 Cholinesterase activity < 50% of normal has been associated with significant exposure to an anticholinesterase agent. Cholinesterase activity <25% of normal is considered indicative of severe poisoning. 5 Previous studies have demonstrated that cholinesterase activity differs among regions of the central nervous system. Miniature swine have twice the cholinesterase activity in the cerebellum as in the cerebral cortex. 6 The acetylcholinesterase activity in the cerebral cortex is about two-thirds lower than that in the cerebellum of guinea pigs but is about the same in both regions for the rat and monkey. 1 In rabbits, the retina has lower acetylcholinesterase activity than do regions of the brain. The cerebellum, occipital lobe, and parietal lobe have similar activities, which are between those for the retina and those for the temporal lobe. The frontal lobe has acetylcholinesterase activity up to twice that of other regions of the brain. 4 Previous work 2,3,8 measuring cholinesterase activity was performed using homogenates of entire brains. However, when submitting samples from large animals such as horses and cows, it is common practice for the referring veterinarian to only submit part of the brain. Because cerebral tissue appears similar regardless of the area sampled, the diagnostician often does not know which part of the brain is being tested. Therefore, the cholinesterase activity of the sample could possibly differ from the normals established using whole brain even if the animal has not been exposed to an anticholinesterase agent. The purpose of this study was to measure the total cho

The Diagnostic Approach and Public Health Implications of Phorate Poisoning In a California Dairy Herd

Within an hour of the planned feeding of a group of 300 Holstein cattle, a large number of cattle developed tremors, diarrhea, weakness, and paralysis. All cows exposed to the feed, a total of 159, died within 24 hours despite treatment attempts with atropine in approximately 100 animals. An additional 8 exposed animals were culled within a week. A thorough investigation demonstrated the accidental mixing of phorate into the total mixed ration instead of the intended mineral mix. Diagnostics confirming phorate exposure in deceased animals included brain cholinesterase determinations and the analysis of liver, rumen content, milk, and feed for phorate. Phorate is a restricted-use organophosphorus pesticide commonly used in US agriculture because of target pest efficacy, cost, and availability. Even with known human, animal, and ecological risks, organophosphorus pesticides remain the most widely used insecticides in the world today. This necessitates awareness about how to identify pesticide exposure in food animals and the corresponding public health risks for humans, including the potential for meat and milk residues and exposure in children. This report describes a dairy’s catastrophic loss of 167 cows caused by human error and assesses the public health implications therein. Veterinary diagnosticians, public health officials, and veterinarians must be prepared to collaborate in order to advise clients on case work-up, management, and preventive measures.